Biology Reference
In-Depth Information
sex of medaka progenies. Experimental depletion of PGCs during the early
embryonic stage induced the production of male progenies alone in medaka
(Slanchev et al., 2005), pearl danio (Saito et al., 2008) and zebrafi sh (Siegfried
and Nusslein-Volhard, 2008). However, the experimental knockdown of
Cxcr4,
the chemo-PGCs attractant receptor gene in medaka by Kurokawa
et al. (2007) has shown that the GCSSCs are pre-disposed toward male
development and the presence of PGCs is essential for sustenance of sexual
dimorphism (Pandian, 2011). During recent years, many publications have
demonstrated the critical role played by the maternal genes and their
products controlling the early embryonic events including DNA repair
and germ cell development (e.g., Abrams and Mullins, 2009; Lindeman
and Pelegri, 2010). In teleost fi shes, the Yolk Syncytial Layer (YSL) has
been considered as extra-embryonic (Sadler, 2004). It is now known that
some descendants of each of these tissues are incorporated into the adult
zebrafi sh (Oteiza et al., 2008). Describing a family of 10 genes
zgc
, Hong
et al. (2010) have found that about four of them protect the embryo and
the others presumably signal the formation of mesoderm and endoderm;
indeed Krens et al. (2008) have identifi ed
ERK1
genes as responsible for
dorso-ventral patterning and subsequent embryonic cell migration and
ERK2
for cell migration and differentiation, and patterning of mesoderm.
In fact maternal gene products continue to play a role in embryonic
development even upto organogenesis (Ryu et al., 2005). Many of these
recent fi ndings suggest that the germ cell supporting somatic cells in the
gonad autonomously activate male genotype but the germ cells activate
the differentiation of female phenotype by sending signals to repress male
pre-disposition and maintain feminization. Thus it is the 'intimate cross-
talk' (Tanaka et al., 2008), and interplay between the PGCs and somatic
supporting cells that seem to determine sex and subsequent differentiation
(see Pandian, 2011).
It must also be indicated that not all the PGCs in the fi sh ovary undergo
the asymmetric mitosis to produce one of their daughter cells to become the
OSC and the other to further undertake cystic division. As the oogenesis
advances in embryonic gonad in
O. latipes
, for instance some PGCs, instead
of forming the cyst and undergoing meiosis, undergo mitotic division.
These PGCs are histologically identifi able by their large size (~ 20 µm in
diameter), large nucleus (6-10 µm) and relatively little cytoplasm, i.e., a high
nuclear cytoplasmic ratio (see Xu et al., 2010). Germ line specifi c marker
proteins such as nanos, vasa, tudor can also be used as reliable markers
(Aoki et al., 2008; see also Table 22). Randomly scattered over the entire
embryonic gonad, “these OSCs persist throughout gonadal development,
providing an inexhaustible source of cells for oogenesis” (Saito and Tanaka,
2009). Table 23 lists landmark developments in identifi cation, isolation
and use of PGCs, SSCs and OSCs to generate allogenics and xenogenics.
